Sentences with phrase «cells called microglia»

In the latest issue of the Journal of Clinical Investigation, available today online, Dr. Farese and his team show how a protein called progranulin prevents a class of cells called microglia from becoming «hyperactive.»

LA JOLLA — Scientists have, for the first time, characterized the molecular markers that make the brain's front lines of immune defense — cells called microglia — unique.

In the brain, a synapse (orange) is seen being wrapped around and attacked by immune cells called microglia (green), leading to synapse loss.

Immune cells called microglia activate as part of the body's inflammatory response, so the researchers used a brain imaging technique to measure a substance that increases in activated microglia.

This process allows specialized Pac - Man — like brain cells called microglia to engulf the targeted synapses, paving the way for more precise brain wiring.

In the present work, the teams led by Michael Ewers (ISD) and EMBO Member Christian Haass (DZNE) focussed on the TREM2 protein, which functions in specialized brain immune cells called microglia that clear toxic material resulting from nerve cell injury.

Looking for immune abnormalities throughout the lifespan of the mice, the group found that most immune system components stayed the same in number, but a type of brain - resident immune cells called microglia that are known first responders to infection begin to divide and change early in the disease.

And researchers must figure out how to build in some core features: the necessary blood vessels, immune - system cells called microglia and connections from other brain regions, such as the thalamus and cerebellum.

What's more, these mice's brains looked inflamed under the microscope, full of immune cells called microglia that were still revved up 30 and 60 days after infection.

Not exact matches

One key gene encodes the making of a receptor called TREM2, a docking site for molecules on the surface of microglia and other innate immune cells.

Our brains normally contain specialized cells, called microglia, that defend against injury or infection.

A low - fat diet in combination with limited caloric consumption prevents activation of the brain's immune cells — called microglia — in aging mice, shows research published today in Frontiers in Molecular Neuroscience.

The brains of mice fed a high glycemic index diet have greater numbers of activated immune cells (shown in red and green) called microglia.

One drug, Protolin, contains bacterial components that rev up immune - system cells in the brain, called microglia, to chew through the beta - amyloid.

Microglia surround TDP -43-filled neurons and turned on genes to make proteins that help them attach to the sick cells and induce a process called phagocytosis that envelops the mutant proteins for disposal.

As luck would have it, cells in the brain called microglia act as the brain's street sweeper, zapping infectious agents, damaged cells, and, importantly, protein tangles and plaques that are thought to cause dementia.

«The activity of the microglia is stimulated by dying brain cells, not by the deposits of amyloid proteins, called plaques, which also occur in Alzheimer's disease,» Haass notes.

TREM2 is segregated by certain immune cells of the brain — called microglia — and thus reflects their activity.

The mass die - off of nerve cells in the brains of people with Alzheimer's disease may largely occur because an entirely different class of brain cells, called microglia, begin to fall down on the job, according to a new study by researchers at the Stanford University School of Medicine.

Two related papers with contributions from Huaxi Xu, Ph.D., the Jeanne and Gary Herberger Chair of Neuroscience and Aging Research at Sanford Burnham Prebys Medical Discovery Institute (SBP), show that a protein called TREM2 helps microglia survive and respond more strongly to damaging material like amyloid and cell debris.

Specialized glial cells - called «microglia» - serve as a resident immune system cells in the brain, activating in response to damage.

Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem cells, stromal cells, haematopoietic stem cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters

And the third major thing that I think we've discovered is that the immune cell of the eye, which is called the microglia; it serves a special function in the maintenance of the health of the retina.

Besides keeping microglia at bay, less PLSCR1 resulted in reduced production of inflammatory molecules called cytokines, whose typical role is to recruit more immune cells to the fight.

The study specifically targets two different types of brain cells, called microglia and astrocytes, that work to keep the immune system in check and clear out old and damaged cells, preventing disease.

Moreover, the idea that the brain was isolated from immune reactions was challenged long ago by insights about microglia cells, a type of macrophage which resides in the brain, engulfs antigens, and produces pro-inflammatory signaling molecules called cytokines.